肺腺癌（LUAD）是一种高度致命的肺癌。尽管治疗方法取得了进步，但由于 LUAD 的攻击性行为，管理 LUAD 仍然具有挑战性。最近的研究表明，多种分子途径，包括铁氧还蛋白 1 (FDX1) 的失调，在 LUAD 进展中发挥作用。 FDX1 是细胞氧化还原反应和能量代谢中的关键蛋白质，与多种癌症有关。然而，其在 LUAD 发生过程中的确切作用尚不完全清楚。我们通过分析铁氧还蛋白 1 (FDX1) 在 LUAD 组织中的表达及其对患者生存的影响，研究了铁氧还蛋白 1 (FDX1) 在 LUAD 进展中的作用。进行功能测定以评估 FDX1 过表达对 LUAD 细胞增殖、迁移和侵袭的影响。采用异种移植模型来评估 FDX1 过表达的 LUAD 细胞的致瘤潜力。通过针对 G 蛋白调节神经突生长诱导物 2 (GPRIN2)/PI3K 信号通路的耗竭实验，获得了对 FDX1 调节的机制见解。FDX1 表达在 LUAD 组织中下调，与患者生存期缩短相关。 FDX1的过表达在体外抑制LUAD细胞增殖、迁移和侵袭，并在体内抑制肿瘤发生。从机制上讲，GPRIN2/PI3K 信号通路与 FDX1 调节有关，因为 GPRIN2 的耗竭逆转了 FDX1 过表达对细胞功能的影响。我们的研究结果强调 FDX1 作为 LUAD 中的潜在肿瘤抑制因子，通过调节 GPRIN2/PI3K 信号通路发挥作用。这些结果表明 FDX1 作为 LUAD 治疗的一个有前途的治疗靶点，值得进一步研究其临床相关性。© 2024。作者。

Lung adenocarcinoma (LUAD) is a highly lethal form of lung cancer. Despite advancements in treatments, managing LUAD is still challenging due to its aggressive behavior. Recent studies indicate that various molecular pathways, including the dysregulation of ferredoxin 1 (FDX1), play roles in LUAD progression. FDX1, a crucial protein in cellular redox reactions and energy metabolism, has been linked to several cancers. However, its exact role in the development of LUAD is not yet fully understood.We investigated the role of ferredoxin 1 (FDX1) in LUAD progression through analysis of its expression in LUAD tissues and its impact on patient survival. Functional assays were performed to assess the effects of FDX1 overexpression on LUAD cell proliferation, migration, and invasion. A xenograft model was employed to evaluate the tumorigenesis potential of LUAD cells with FDX1 overexpression. Mechanistic insights into FDX1 regulation were gained through depletion experiments targeting the G protein-regulated inducer of neurite outgrowth 2 (GPRIN2)/PI3K signaling pathway.FDX1 expression was down-regulated in LUAD tissues, correlating with shorter patient survival. Overexpression of FDX1 suppressed LUAD cell proliferation, migration, and invasion in vitro, and inhibited tumorigenesis in vivo. Mechanistically, the GPRIN2/PI3K signaling pathway was implicated in FDX1 regulation, as depletion of GPRIN2 reversed the effects of FDX1 overexpression on cellular functions.Our findings highlight FDX1 as a potential tumor suppressor in LUAD, acting through modulation of the GPRIN2/PI3K signaling pathway. These results suggest FDX1 as a promising therapeutic target for LUAD treatment, warranting further investigation into its clinical relevance.© 2024. The Author(s).